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MBBS Y5 > Medicine - Respiratory > Flashcards

Medicine - Respiratory Flashcards

1
Q

how can lung cancer be classified histologically? what % of total lung cancers are each of them?

A
  • non-small cell lung cancer, 80%| - small cell lung cancer (SCLC), 20%
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2
Q

2 types of non-small cell lung cancer?

A
  • squamous cell carcinoma| - adenocarcinoma (more likely in a non-smoker)
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3
Q

which type of lung cancer can give rise to paraneoplastic syndromes? how?

A
  • SCLC| - the cells have granules which secrete neuroendocrine hormones
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4
Q

presentation of lung cancer?

A

NAME?

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5
Q

which lymph nodes are enlarged first typically in lung cancer?

A

supraclavicular ones

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6
Q

first line investigation in lung cancer? what are the findings?

A

NAME?

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7
Q

investigations in lung cancer?

A

NAME?

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8
Q

when is surgical management used in lung cancer? what types are there?

A

NAME?

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9
Q

management of SCLC? prognosis?

A

NAME?

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10
Q

palliative treatment options for lung cancer?

A

NAME?

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11
Q

complications of lung cancer relating to compression and hormone secretion?

A

compression: - recurrent laryngeal palsy- phrenic nerve palsy- SVCO- horner’s syndrome hormonal:- SIADH- cushing’s syndrome - hypercalcaemia - limbic encephalitis - lambert-eaton myasthenic syndrome

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12
Q

how can lung cancer cause nerve palsy? which nerves are commonly affected?

A

NAME?

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13
Q

presentation of SVC obstruction?

A
  • facial swelling - difficulty breathing - distended veins in neck and upper chest- pemberton’s sign
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14
Q

what is pemberton’s sign? is it significant?

A
  • raising the hands over the head causes facial congestion and cyanosis - medical emergency!
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15
Q

how can lung cancer cause horner’s syndrome?

A

pancoast tumour compressing the sympathetic ganglion

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16
Q

presentation of horner’s syndrome?

A

triad:- partial ptosis - anhidrosis- miosis

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17
Q

what is a pancoast’s tumour?

A

tumour in the apex of the lung

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18
Q

how can lung cancer cause SIADH? key finding on bloods?

A
  • SCLC tumour secreting ectopic ADH| - hyponatraemia
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19
Q

how can lung cancer cause cushing’s syndrome?

A

SCLC secreting ectopic ACTH

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20
Q

how can lung cancer cause hypercalcaemia?

A

squamous cell carcinoma (non-SCLC) secreting ectopic PTH

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21
Q

describe limbic encephalitis

A

NAME?

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22
Q

pathophysiology of lambert-eaton myasthenic syndrome?

A

antibodies created against SCLC cells but which also happen to attack voltage-gated Ca channels in motor neurones

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23
Q

presentation of lambert-eaton myasthenic syndrome?

A

NAME?

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24
Q

top differential for lambert-eaton myasthenic syndrome?

A
  • myasthenia gravis| - onset is more insidious and symptoms less pronounced in lambert-eaton
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25
Q

which cells are affected in mesothelioma?

A

mesothelial cells of the pleura

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26
Q

biggest risk factor for mesothelioma?

A
  • asbestos inhalation / exposure| - latent period as long as 45 years
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27
Q

management of mesothelioma? prognosis?

A
  • palliative chemotherapy| - very poor
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28
Q

finding on CXR in pneumonia?

A

consolidation

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29
Q

what is hospital acquired pneumonia (HAP)?

A

pneumonia which develops >48h after hospital admission

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30
Q

different types of pneumonia?

A

NAME?

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31
Q

presentation of pneumonia?

A

NAME?

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32
Q

findings in a set of obs in pnuemonia?

A

NAME?

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33
Q

lung signs on examination in pneumonia?

A

NAME?

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34
Q

describe bronchial breathing

A

harsh breathing, equally loud on inspiration and expiration

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35
Q

scoring system for severity and risk of mortality from pneumonia in hospital? in community?

A
  • CURB-65 in hospital| - urea not checked out of hospital (CRB-65)
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36
Q

different parts of CURB-65?

A
  • Confusion, new onset- Urea >7- RR >30- BP <90 systolic, <60 diastolic - 65 or above years old
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37
Q

which CURB-65 score determines which treatment?

A
  • 0-1 = home treatment - 2 = hospital admission - 3 or more = ICU care
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38
Q

commonest bacterial causes of pneumonia?

A
  • strep pneumoniae (50%)| - H. influenzae (20%)
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39
Q

which organism causes pneumonia in immunocompromised / COPD patients?

A

moraxella catarrhalis

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40
Q

which organisms cause pneumonia in CF patients?

A
  • pseudomonas aeruginosa| - staph aureus
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41
Q

who is at higher risk of pneumonia from pseudomonas aeruginosa?

A
  • CF patients| - bronchiectasis patients
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42
Q

define atypical pneumonia

A

pneumonia caused by an organism which cannot be cultured in the normal way or detected by gram stain

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43
Q

which ABx should be used on atypical pneumonia?

A

macrolides

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44
Q

organisms which cause atypical pneumonia?

A

NAME?

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45
Q

how is legionella pneumophila contracted? how does it present?

A

NAME?

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46
Q

how does mycoplasma pneumoniae infection present?

A
  • mild pneumonia - erythema multiforme (“target” lesions)- warm-type AIHA
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47
Q

which demographic typically gets chlamydia pneumoniae infection? how does it present?

A
  • school aged children - chronic cough and wheeze- (be careful because this is a common presentation!)
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48
Q

another name for coxiella burnetii infection? how does it spread?

A
  • Q fever- animal bodily fluids- e.g. “farmer with a flu”
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49
Q

Legions of psittaci MCQs: 5 causes of atypical pneumonia?

A

NAME?

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50
Q

which organism could cause a fungal pneumonia?

A

pneumocystis jiroveci

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51
Q

which patients are at risk of pnuemocystis jiroveci pneumonia?

A
  • immunocompromised| - e.g. HIV+ with low CD4 count
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52
Q

presentation of fungal pneumonia?

A

NAME?

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53
Q

management of fungal pneumonia?

A
  • co-trimoxazole (trimethoprim + sulfamethoxazole)
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54
Q

how can fungal pneumonia be prevented?

A

all HIV+ pts with CD4 count <200 are given prophylactic co-trimoxazole alongside their regular ART

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55
Q

investigations for pneumonia? findings?

A
  • CXR (consolidation)- FBC (raised WCC)- UEs (urea for CURB-65)- CRP (raised)
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56
Q

extra investigations done in severe pneumonia?

A

NAME?

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57
Q

when might CRP be low in pneumonia? why?

A
  • immunocompromised patients| - they can’t mount an immune response
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58
Q

management of severe pneumonia?

A

NAME?

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59
Q

management of mild CAP?

A

5 day oral course of either:- amoxicillin - macrolide

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60
Q

management of mod-sev CAP?

A

7-10 day course of BOTH amoxicillin AND a macrolide

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61
Q

SPELD: complications of pneumonia?

A

NAME?

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62
Q

3 outcome measures of lung function tests?

A

NAME?

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63
Q

in spirometry, what is reversible testing?

A

giving a bronchodilator (salbutamol) before doing the breathing exercises

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64
Q

what is FEV1? when is it reduced?

A
  • forced expiratory volume in 1 second- volume of air a person can forcefully exhale in 1 second- reduced in lung obstruction
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65
Q

what is FVC? when is it reduced?

A

NAME?

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66
Q

how is obstructive lung disease diagnosed?

A

FEV1/ FVC <0.75

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67
Q

examples of obstructive lung disease?

A

NAME?

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68
Q

FEV1/FVC in restrictive lung disease? explain this

A
  • FEV1/FVC >0.75 (normal or raised)| - they’re both equally reduced, so the ratio doesn’t change
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69
Q

describe restrictive lung disease

A

restriction in lung’s ability to expand

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70
Q

examples / causes of restrictive lung diseases?

A

NAME?

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71
Q

when is peak flow (PEFR) useful?

A

to demonstrate obstruction in asthma

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72
Q

how is peak flow measured?

A
  • stand tall and take a deep breath in- make a good seal with the device- blow hard and fast ;)- 3 attempts, take the best one
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73
Q

how is the peak flow result interpreted?

A
  • predicted peak flow obtained from chart| - record it as % of actual over predicted
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74
Q

factors taken into account in predicted peak flow?

A

NAME?

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75
Q

what is asthma?

A

chronic inflammatory condition where there is bronchoconstriction in exacerbations

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76
Q

how does asthma cause obstruction? is this reversible?

A

NAME?

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77
Q

how is obstruction in asthma reversed?

A

bronchodilator (salbutamol)

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78
Q

triggers of bronchoconstriction in asthma?

A

NAME?

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79
Q

presentation of asthma?

A

NAME?

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80
Q

what is heard on auscultation in asthma?

A

bilateral widespread polyphonic wheeze

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81
Q

what are the first line investigations in asthma diagnosis according to NICE?

A
  • fractional exhaled nitric oxide (FeNO)| - spirometry with bronchodilator reversibility
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82
Q

second line investigations in asthma diagnosis?

A
  • peak flow variability| - direct bronchial challenge with histamine / methacholine
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83
Q

full form of SABA? how long does the effect of a SABA last? what is the inhaler commonly called? example?

A
  • short acting beta 2 agonist- only lasts 1-2 hours- “reliever”, “rescue”- salbutamol
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84
Q

example of an ICS? how do they work? what is the inhaler commonly called?

A
  • beclometasone, budesonide, fluticasone - reduces inflammation in airway- “maintenance”, “preventer”
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85
Q

full form of LABA? example? what is the difference between LABA and SABA?

A
  • long acting beta 2 agonist- salmeterol- same MOA but LABA lasts much longer
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86
Q

full form of LAMA? example? how does it work?

A

NAME?

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87
Q

full form of LTRA? example? how does it work?

A

NAME?

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88
Q

what are the effects of leukotrienes?

A

NAME?

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89
Q

how does theophylline work?

A
  • relaxes bronchial smooth muscle| - reduces inflammation
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90
Q

why does theophylline need to be monitored? how is it monitored?

A
  • narrow therapeutic window, can cause toxicity- check blood theophylline levels 5 days after starting treatment - check 3 days after each dose change
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91
Q

what does MART stand for in asthma treatment? why is it useful?

A

NAME?

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92
Q

step 1 in NICE asthma treatment ladder?

A

SABA (salbutamol), PRN

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93
Q

step 2 in NICE asthma treatment ladder?

A

add low dose ICS (beclometasone)

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94
Q

step 3 in NICE asthma treatment ladder? how does SIGN/BTS differ here?

A
  • NICE: add LABA (salmeterol)| - SIGN/BTS: add LTRA (montelukast)
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95
Q

step 4 in NICE asthma treatment ladder?

A

consider adding one of these:- LTRA (montelukast)- theophylline- PO SABA (salbutamol)- LAMA (tiotropium)

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96
Q

step 5 in NICE asthma treatment ladder?

A

increase ICS from low dose to high dose

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97
Q

step 6 in NICE asthma treatment ladder?

A

add oral steroids

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98
Q

other than regular medication, what else is part of asthma management?

A

NAME?

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99
Q

presentation of acute asthma exacerbation?

A

NAME?

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100
Q

signs on auscultation in acute asthma exacerbation?

A
  • symmetrical expiratory wheeze| - “tight” chest sounds (reduced air entry)
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101
Q

how are acute asthma exacerbations graded?

A

NAME?

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102
Q

features of a moderate acute asthma exacerbation?

A
  • peak flow 50-75% of predicted- normal speech- RR <25/min- pulse <110/min
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103
Q

features of a severe acute asthma exacerbation?

A
  • peak flow is 33-50% of predicted- RR >25- HR >110- unable to complete a sentence
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104
Q

features of a life-threatening acute asthma exacerbation?

A
  • peak flow isn <33% of predicted- O2 sats <92%- becoming tired- silent chest (no wheeze)- haemodynamic instability (shock)
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105
Q

management of a moderate acute asthma exacerbation?

A
  • nebulised salbutamol 5mg, repeat as much as needed- nebulised ipratropium bromide - PO pred or IV hydrocortisone for 5 days - ABx if bacterial cause suspected
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106
Q

management of a severe acute asthma exacerbation?

A
  • O2 to maintain sats of 94-98%- aminophylline infusion - consider IV salbutamol
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107
Q

management of a life-threatening acute asthma exacerbation?

A

NAME?

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108
Q

ABG findings in an acute asthma exacerbation? why?

A
  • respiratory alkalosis (drop in CO2 from tachypnoea)| - normal pCO2 means they are tiring and retaining more CO2
109
Q

why is respiratory acidosis a worrying finding on ABG in asthma?

A

it means they have high CO2 because they’re not blowing any of it off

110
Q

how is treatment response monitored in acute asthma exacerbations?

A

NAME?

111
Q

which electrolyte needs to be monitored in patients on salbutamol? why?

A
  • serum K+| - salbutamol causes K+ to move from blood into cells
112
Q

define COPD

A

non-reversible, long term obstruction in air flow through the lungs caused by damage to lung tissue

113
Q

presentation of COPD?

A

NAME?

114
Q

main risk factor for COPD?

A

smoking

115
Q

how can breathlessness be assessed?

A

MRC dyspnoea scale

116
Q

describe the 5 grades of the MRC dyspnoea scale

A
  • 1 = breathless on strenuous exercise- 2 = breathless on walking uphill- 3 = breathessness that slows walking on the flat- 4 = stops to catch breath after walking 100m on the flat- 5 = unable to leave the house due to breathlessness
117
Q

how is COPD diagnosed?

A

both of:- clinical picture - spirometry showing: FEV1/FVC <0.7

118
Q

results of spirometry reversibility testing in COPD?

A

no dramatic reversal with salbutamol

119
Q

how can the severity of obstruction in COPD be assessed?

A

look at the FEV1 compared to the predicted value

120
Q

investigations (other than spirometry) and findings in COPD?

A

NAME?

121
Q

what is TLCO?

A

transfer factor for carbon monoxide

122
Q

non-drug management of COPD?

A

NAME?

123
Q

step 1 in drug management of COPD?

A

SABA (salbutamol) or SAMA (ipratropium)

124
Q

step 2 in COPD management with NO features of asthma / response to steroids?

A
  • combined inhaler| - includes LABA and a LAMA
125
Q

which add-on meds can be used in COPD management?

A

NAME?

126
Q

what determines step 2 of COPD medical management?

A
  • whether they have features of asthma| - whether it is steroid-responsive
127
Q

step 2 in COPD management with features of asthma / response to steroids? if this fails?

A

NAME?

128
Q

indications for long-term O2 therapy use in COPD?

A

NAME?

129
Q

significant contraindication for O2 therapy?

A

smoking! fire hazard

130
Q

presentation of COPD exacerbation?

A

acute worsening of:- cough - SOB- sputum production - wheeze

131
Q

what causes a COPD exacerbation?

A

viral / bacterial infection

132
Q

ABG findings in someone acutely retaining CO2? why? what is this called?

A

NAME?

133
Q

ABG findings in someone chronically retaining CO2? why?

A
  • raised bicarbonate| - kidneys compensate for the acid by producing something alkaline
134
Q

ABG findings in type 1 resp failure?

A
  • low pO2| - normal pCO2
135
Q

ABG findings in type 2 resp failure?

A
  • low pO2| - high pCO2
136
Q

investigations in COPD exacerbation?

A

NAME?

137
Q

why does O2 therapy need careful monitoring if someone is retaining CO2? how is it done?

A

NAME?

138
Q

target O2 sats in CO2 retainers?

A

88-92% titrated by venturi mask

139
Q

target O2 sats in COPD patient NOT retaining CO2?

A

> 94%

140
Q

treatment of COPD exacerbation at home?

A
  • pred 30mg for 7-14 days - regular inhalers / nebulisers - ABx if signs of infection
141
Q

treatment of COPD exacerbation in hospital?

A

NAME?

142
Q

management of COPD exacerbation not responding to first line treatment?

A

NAME?

143
Q

what are the types of non-invasive ventilation (NIV)?

A
  • BiPAP| - CPAP
144
Q

what does BiPAP stand for? when is it indicated?

A
  • bilevel positive airway pressure - type 2 resp failure - patient must have resp acidosis despite medication
145
Q

contraindications for BiPAP?

A
  • untreated pneumothorax| - any other serious pathology affecting face / airway / GI tract
146
Q

imaging done before BiPAP? why?

A
  • CXR| - to rule out pneumothorax
147
Q

what does CPAP stand for?

A

continuous positive airway pressure

148
Q

indications for CPAP?

A

NAME?

149
Q

describe interstitial lung disease (ILD)

A

NAME?

150
Q

diagnostic investigation for ILD? findings?

A
  • high-res CT (HRCT)| - ground glass appearance
151
Q

prognosis in ILD?

A
  • poor| - the fibrosis is irreversible
152
Q

management of ILD? hint: supportive

A

NAME?

153
Q

what is idiopathic pulmonary fibrosis?

A
  • pulmonary fibrosis without a clear cause| - type of interstitial lung disease
154
Q

typical demographic for idiopathic pulmonary fibrosis?

A

those aged >50 years old

155
Q

presentation of idiopathic pulmonary fibrosis?

A
  • insidious onset over >3 months- SOB- dry cough
156
Q

signs O/E in idiopathic pulmonary fibrosis?

A
  • bibasal fine inspiratory crackles| - finger clubbing
157
Q

prognosis in idiopathic pulmonary fibrosis?

A
  • poor| - life expectancy of 2-5 years
158
Q

2 medications which can slow progression of idiopathic pulmonary fibrosis?

A
  • pirfenidone| - nintedanib
159
Q

drugs which can cause pulmonary fibrosis?

A

NAME?

160
Q

which conditions can pulmonary fibrosis be secondary to?

A

NAME?

161
Q

what is the other name for extrinsic allergic alveolitis (EAA)?

A

hypersensitivity pneumonitis

162
Q

describe EAA?

A

NAME?

163
Q

investigation in EAA? findings

A

NAME?

164
Q

what does bronchoalveolar lavage involve? when is it used?

A

NAME?

165
Q

4 specific causes of EAA? what is each one called?

A
  • bird droppings (bird-fanciers lung)- mould spores in hay (farmers lung)- mushroom antigens (mushroom workers lung)- mould spores in barley (malt workers lung)
166
Q

what is asbestosis?

A

lung fibrosis caused by inhaling asbestos

167
Q

conditions caused by asbestos inhalation?

A

NAME?

168
Q

what is a pleural effusion?

A

collection of fluid in the pleural space

169
Q

what is an exudative pleural effusion?

A

there is >3g/L (high) protein in the fluid

170
Q

causes of exudative pleural effusion? (hint: inflammation)

A

think inflammation:- lung cancer- pneumonia - RA- TB

171
Q

what is a transudative pleural effusion?

A

there is <3g/L (low) protein in the fluid

172
Q

causes of transudative pleural effusion? (hint: fluid shift)

A

think of things causing fluid to move:- CCF- hypoalbuminaemia (nephrotic syndrome)- hypothyroidism - Meig’s syndrome

173
Q

what is Meig’s syndrome?

A

R-sided pleural effusion with ovarian malignancy

174
Q

presentation (including O/E) of pleural effusion?

A

NAME?

175
Q

findings on CXR in pleural effusion?

A

NAME?

176
Q

what can be tested for in a sample of pleural effusion fluid?

A

NAME?

177
Q

management of pleural effusion?

A

NAME?

178
Q

what is empyema? when should you suspect it?

A
  • an infected pleural effusion| - when someone comes in with pneumonia-like signs but they are not responding to ABx
179
Q

findings on aspiration of empyema?

A
  • pus- acidic pH (<7.2)- low glucose- high LDH
180
Q

management of empyema?

A
  • chest drain| - ABx
181
Q

describe pneumothorax

A

air in the pleural space separating the lung from the chest wall

182
Q

causes of pneumothorax?

A

NAME?

183
Q

what are the iatrogenic causes of pneumothorax?

A

NAME?

184
Q

which lung pathologies could cause a pneumothorax?

A

NAME?

185
Q

investigations in pneumothorax?

A
  • erect CXR| - CT thorax ( for smaller ones not seen on CXR)
186
Q

management of pneumothorax where there is no SOB and there is a <2cm rim of air on CXR?

A

NAME?

187
Q

management of pneumothorax where there is SOB +/- rim of air is >2cm on CXR?

A

NAME?

188
Q

what is a tension pneumothorax? what causes it?

A

NAME?

189
Q

signs (including O/E) of tension pneumothorax?

A

NAME?

190
Q

main complication of tension pneumothorax?

A

cardiorespiratory arrest

191
Q

management of tension pneumothorax?

A
  • insert a large bore cannula into the 2nd IC space in the midclavicular line - once some pressure is relieved, insert chest drain- do NOT wait for investigations
192
Q

describe the borders of the “triangle of safety”. why is this space important?

A
  • 5th IC space- mid-axillary line - anterior axillary line - this is where chest drains are inserted
193
Q

what is a pulmonary embolism (PE)?

A
  • a blood clot in the pulmonary arteries| - usually secondary to a DVT which has travelled
194
Q

risk factors for developing VTE?

A
  • recent surgery - long haul flights - pregnancy- oestrogen therapy- malignancy (hypercoagulable state!)- polycythaemia - SLE - thrombophilia
195
Q

what prophylaxis is offered to patients at risk of VTE?

A
  • LMWH (enoxaparin)| - compression stockings
196
Q

main contraindication for compression stockings?

A

peripheral arterial disease

197
Q

contraindications for LMWH?

A
  • active bleeding| - anyone on warfarin / NOAC (anticoag)
198
Q

presentation of PE?

A
  • cough +/- blood - pleuritic chest pain- hypoxia - tachycardia - tachypnoea - low grade fever - haemodynamic instability- hypotension
199
Q

what can be calculated if you suspect a PE?

A

wells score

200
Q

which factors are taken into account for wells score?

A

NAME?

201
Q

how is the wells score outcome interpreted in suspected PE?

A
  • PE likely: CT pulmonary angiogram (CTPA)| - PE unlikely: D-dimer
202
Q

what is the next investigation in suspected PE if D-dimer is positive? hint: different for renal impairment

A
  • CTPA| - if renal impairment: VQ scan
203
Q

diagnostic investigations for PE?

A
  • CTPA| - VQ scan (ventilation-perfusion)
204
Q

what does the ABG pH show in PE? why?

A

NAME?

205
Q

2 main causes of resp alkalosis?

A
  • PE| - hyperventilation syndrome
206
Q

supportive management in PE?

A

NAME?

207
Q

medical management of PE?

A
  • IV fluids / oxygen if needed- start off with rivaroxaban + LMWH (dalteparin)- then long-term anticoag (warfarin or NOAC) for 3 months - carry on for longer if unsure of cause / malignancy present
208
Q

is D-dimer sensitive / specific to VTE?

A
  • sensitive but not specific| - if low, unlikely to be VTE but if raised can be something else
209
Q

causes of a raised D-dimer?

A

NAME?

210
Q

management of a massive PE with haemodynamic instability? which agents can be used for this?

A

NAME?

211
Q

causes of pulmonary hypertension?

A

NAME?

212
Q

presentation of pulmonary HTN?

A

NAME?

213
Q

investigations for pulmonary HTN?

A

NAME?

214
Q

ECG changes in pulmonary HTN?

A
  • RV hypertrophy - R axis deviation- RBBB
215
Q

CXR changes seen in pulmonary HTN?

A
  • dilated pulmonary arteries| - RV hypertrophy
216
Q

prognosis in pulmonary HTN?

A
  • poor| - 30% life expectancy at 5 years post-diagnosis
217
Q

treatment for primary pulmonary HTN?

A
  • IV prostanoids (epoprostenol)- endothelial receptor antagonists (macitentan)- phosphodiesterase-5 inhibitors (sildenafil)
218
Q

complications of pulmonary HTN?

A

NAME?

219
Q

management of secondary pulmonary HTN?

A

manage the underlying cause

220
Q

what is sacrdoidosis?

A
  • granulomatous inflammatory condition| - gives chest signs and extrapulmonary signs
221
Q

what do the granulomas in sarcoidosis contain?

A

macrophages

222
Q

demographics affected by sarcoidosis?

A
  • 2 spikes in incidence- young adulthood and 60s - F>M- Black people more affected
223
Q

organs affected by sarcoidosis? (hint: literally everything)

A

NAME?

224
Q

what can sarcoidosis cause in the lungs?

A

NAME?

225
Q

what can sarcoidosis cause in the liver?

A

NAME?

226
Q

what can sarcoidosis cause in the eyes?

A

NAME?

227
Q

what can sarcoidosis cause on the skin?

A

NAME?

228
Q

systemic signs of sarcoidosis?

A

NAME?

229
Q

what can sarcoidosis cause in the heart?

A

NAME?

230
Q

what can sarcoidosis cause in the kidneys?

A

NAME?

231
Q

what can sarcoidosis cause in the nervous system? (hint: split into central and peripheral)

A

central: - diabetes insipidus (pituitary)- encephalopathy peripheral:- bell’s palsy- mononeuritis multiplex

232
Q

what can sarcoidosis cause in the bones?

A

NAME?

233
Q

what is lofgren’s syndrome?

A

a specific presentation of sarcoidosis

234
Q

presentation of lofgren’s syndrome? hint: triad

A

NAME?

235
Q

differentials for sarcoidosis?

A

NAME?

236
Q

investigations and findings for sarcoidosis?

A

NAME?

237
Q

findings of blood tests in sarcoidosis?

A
  • raised serum ACE (screening) - raised Ca - raised IL-2 receptor- raised CRP- raised Ig
238
Q

gold standard investigation to diagnose sarcoidosis?

A

biopsy and histology

239
Q

what is seen on histology in sarcoidosis?

A

non-caseating granulomas with epithelioid cells

240
Q

management of asymptomatic / mild sarcoidosis?

A
  • nothing| - resolves spontaneously
241
Q

1st line treatment of symptomatic sarcoidosis? 2nd line?

A
  • PO steroids for 6-24 months - give bisphosphonates concurrently (stops osteoporosis) - 2nd line: methotrexate or azathioprine - lung transplant if severe lung disease
242
Q

prognosis of sarcoidosis?

A
  • good- 60% resolve spontaneously in 6 months - in some patients goes on to cause pul fibrosis / HTN
243
Q

what causes obstructive sleep apnoea (OSA)?

A

collapse of the pharyngeal airway in sleep

244
Q

risk factors for OSA?

A

NAME?

245
Q

features of OSA?

A

NAME?

246
Q

describe an apnoeic episode

A
  • the person stops breathing for a few minutes| - typically unaware of this themselves
247
Q

complications of OSA?

A

NAME?

248
Q

investigations for OSA?

A
  • sleep studies| - done by ENT specialists or sleep clinics
249
Q

management of OSA?

A

NAME?

250
Q

ECG changes seen in PE?

A
  • sinus tachycardia - R-axis deviation- complete / partial RBBB- S waves in lead I- Q waves in lead III- T wave inversion in lead III
251
Q

what is ARDS? explain the pathophysiology of it

A

NAME?

252
Q

risk factors for ARDS? hint: most common first and there’s a LOT

A

NAME?

253
Q

features of ARDS?

A

NAME?

254
Q

signs O/E of ARDS?

A
  • cyanosis| - bilateral fine inspiratory crackles
255
Q

management of ARDS?

A

NAME?

256
Q

differentials for a “white out” on CXR?

A

NAME?

257
Q

differentials for a “white out” on CXR where the trachea is central?

A

NAME?

258
Q

differentials for a “white out” on CXR where the trachea is PULLED towards it?

A

NAME?

259
Q

differentials for a “white out” on CXR where the trachea is PUSHED away from it?

A

NAME?

260
Q

poor prognostic factor in CF?

A

chronic infection with either:- pseudomonas- burkholderia

261
Q

indications for corticosteroids in sarcoidosis?

A

NAME?

262
Q

what is bronchiectasis?

A

permanent dilation of bronchi / bronchioles from chronic infection

263
Q

main causative organisms of pts affected by bronchiectasis?

A

NAME?

264
Q

causes of bronchiectasis?

A

NAME?

265
Q

presentation of bronchiectasis?

A

NAME?

266
Q

findings on spirometry in bronchiectasis?

A

obstructive pattern

267
Q

findings on CXR in bronchiectasis?

A
  • tramlines| - ring shadows
268
Q

features of legionnaire’s disease?

A

NAME?

MBBS Y5 (27 decks)

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